vWF与GPⅡb/Ⅲa在血小板黏附、聚集中的作用及与PCI术并发症的关系

遗传性假血友病因子(vWF)是一种黏附、多聚糖蛋白,分布在血浆、血小板和内皮下,在血小板黏附到内皮下的过程中起着重要作用。GPⅡb/Ⅲa在凝血过程中的血小板黏附和聚集中也起关键作用,血小板激活导致GPⅡb/Ⅲa构型发生变化,继而使GPⅡb/Ⅲa受体与配体纤维蛋白原的结合加强,纤维蛋白原在相邻血小板分子间形成桥梁,导致血小板聚集的加速。经皮冠状动脉介入治疗术后并发症的发生与血小板的激活、血栓形成有关,本文旨在简述vWF和Ⅱb/Ⅲ在血小板黏附和聚集中的作用及其与经皮冠状动脉介入治疗(PCI)术后并发症发生的关系。

The Roles of the von Willebrand Factor and the Platelet Glycoprotein Ⅱ b/Ⅲ a in Platelet Adhesion and Aggregation and the Relationship with the Complications after Percutaneous Coronary Intervention

Von willerbrand factor(vWF) is an adhesive,poly-glycoprotein distributing in plasma,platelet and subendothelium,which plays an important role in adhesive process of platelet to subendothelium.Glycoprotein Ⅱb/Ⅲa(GPⅡb/Ⅲa) also play a key role in the adhesion and aggregation of platelet during coagulation.The activated platelet can result in the changes of GPⅡb/Ⅲa in its conformation,which then intensifies the binding between GPⅡb/Ⅲa and its ligand fibrinogen.Fibrinogen can make bridge between platelets close together,which then accelarates the aggregation of platelets.There is a correlationship of complication after percutaneous coronary intervention(PCI) with platelet activation and thrombus formation.The aim of this article is to review the effect of vWF and GPⅡb/Ⅲa in the platelet adhesion and aggregation and to describe the potential relationship with the complication after PCI.